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- dc.contributor.author
- 김은정
- dc.contributor.author
- 이윤태
- dc.contributor.author
- Huda Y. Zoghbi
- dc.contributor.author
- John D. Fryer
- dc.contributor.author
- 강효진
- dc.contributor.author
- 김경태
- dc.contributor.author
- 김소은
- dc.contributor.author
- 박성준
- dc.contributor.author
- 여지현
- dc.contributor.author
- 이지은
- dc.contributor.author
- 정회윤
- dc.contributor.author
- 최나현
- dc.contributor.author
- 황대희
- dc.date.accessioned
- 2019-08-28T07:41:39Z
- dc.date.available
- 2019-08-28T07:41:39Z
- dc.date.issued
- 2015-02-05
- dc.identifier.issn
- 2045-2322
- dc.identifier.uri
- https://repository.kisti.re.kr/handle/10580/14377
- dc.identifier.uri
- http://www.ndsl.kr/ndsl/search/detail/article/articleSearchResultDetail.do?cn=NART72145526
- dc.language
- eng
- dc.relation.ispartofseries
- Scientific Reports
- dc.title
- Deficiency of Capicua disrupts bile acid homeostasis
- dc.citation.number
- 8272
- dc.subject.keyword
- Capicua (CIC) has been implicated in pathogenesis of spinocerebellar ataxia type 1 and cancer in mammals
- dc.subject.keyword
- however
- dc.subject.keyword
- the in vivo physiological functions of CIC remain largely unknown. Here we show that Cic hypomorphic (Cic-L-/-) mice have impaired bile acid (BA) homeostasis associated with induction of proinflammatory cytokines. We discovered that several drug metabolism and BA transporter genes were down-regulated in Cic-L-/- liver
- dc.subject.keyword
- and that BA was increased in the liver and serum whereas bile was decreased within the gallbladder of Cic-L-/- mice. We also found that levels of proinflammatory cytokine genes were up-regulated in Cic-L-/- liver. Consistent with this finding
- dc.subject.keyword
- levels of hepatic transcriptional regulators
- dc.subject.keyword
- such as hepatic nuclear factor 1 alpha (HNF1α)
- dc.subject.keyword
- CCAAT/enhancer-binding protein beta (C/EBPβ)
- dc.subject.keyword
- forkhead box protein A2 (FOXA2)
- dc.subject.keyword
- and retinoid X receptor alpha (RXRα)
- dc.subject.keyword
- were markedly decreased in Cic-L-/- mice. Moreover
- dc.subject.keyword
- induction of tumor necrosis factor alpha (Tnfα) expression and decrease in the levels of FOXA2
- dc.subject.keyword
- C/EBPβ
- dc.subject.keyword
- and RXRα were found in Cic-L-/- liver before BA was accumulated
- dc.subject.keyword
- suggesting that inflammation might be the cause for the cholestasis in Cic-L-/- mice. Our findings indicate that CIC is a critical regulator of BA homeostasis
- dc.subject.keyword
- and that its dysfunction might be associated with chronic liver disease and metabolic disorders.
- Appears in Collections:
- 7. KISTI 연구성과 > 학술지 발표논문
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